Dear Netters:
I would appreciate somebody help us to make some sense out of an intriguing
result we recently observed. We recently made more than ten independent
lines of transgenic tobacco plants harboring a human gene under the control
of the 35S promoter. We tested some of these lines in their primary (T0)
generation without finding any altered phenotype. We then collected the
seeds, germinated them in the kanamycin-containing medium and tested again
in the T1 generation. Surprisingly, we found that 20 to 50% of these
kanamycin-resistant plants from 9 out of the 10 tested lines exhibited an
dramatically altered phenotype. Assuming that this altered phenotype is
due to the expression of the transgene (we observed no such altered
phenotype in the control lines transformed with the vector without this
human gene), then why did not these plants exhibit the altered phenotype in
the T0 generation? The only possibility that we can think of is that this
altered phenotype requires a high-level expression of this transgene that
can occur only when the gene is in a homozygous state or with a high copy
number in some plants of the T1 generation. Does expression of transgenes
usually behave like this (and so uniformly for almost all independent lines
tested)? Any help would be greatly appreciated.
Zhixiang Chen
MMBB
University of Idaho